ArticleScientific reports2018
A cleavage product of Polycystin-1 is a mitochondrial matrix protein that affects mitochondria morphology and function when heterologously expressed.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
63 citing papers in PubMed, 109 citations in OpenAlex.
- Baseline Characteristics and Patient-Reported Outcomes of ADPKD Patients in the Multicenter TAME-PKD Clinical Trial.Kidney360 · 2020Trial
- RhoA through its various effectors mediate mitochondrial fragmentation in polycystic kidney disease.iScience · 2026Article
- Modeling Complex Developmental Disease: The Case of Polycystic Kidney Disease.Journal of developmental biology · 2026Review
- Polycystin-1 and Cardiac Remodeling: From Mechanotransduction to Clinical Consequences.Circulation research · 2026Review
- Physiological functions and pharmacological targeting of transient receptor potential channels.Pharmacological reviews · 2025Review
- Cleavage of N-terminus of polycystin-1 increases calcium permeability of polycystin-1/2 receptor channel complexes.JCI insight · 2025Article
- Physiologic mechanisms underlying polycystic kidney disease.Physiological reviews · 2025Review
- Metabolic reprogramming in polycystic kidney disease and other renal ciliopathies.EMBO molecular medicine · 2025Review
- Ameliorative Effect of an Anti-MicroRNA-21 Oligonucleotide on Animal and Human Models of Cystic Kidney Disease.Kidney360 · 2025Article
- Eliosin-an alternative product from the HmPKD1 locus is a component of endoplasmic reticulum mitochondria membrane contact sites.PloS one · 2025Article
- The Influence of Non-Pharmacological and Pharmacological Interventions on the Course of Autosomal Dominant Polycystic Kidney Disease.Nutrients · 2024Review
- Kidney Energetics and Cyst Burden in Autosomal Dominant Polycystic Kidney Disease: A Pilot Study.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2024Article
- Acyl-CoA thioesterase 13 (Aging · 2024Article
- Comparative genomics reveals convergent signals associated with the high metabolism and longevity in birds and bats.Proceedings. Biological sciences · 2024Article
- Reprogramming of Energy Metabolism in HumanInternational journal of molecular sciences · 2024Article
- Inhibition of asparagine synthetase effectively retards polycystic kidney disease progression.EMBO molecular medicine · 2024Article
- Leucine-Rich Repeat in Polycystin-1 Suppresses Cystogenesis in a Zebrafish (International journal of molecular sciences · 2024Article
- A synthetic agent ameliorates polycystic kidney disease by promoting apoptosis of cystic cells through increased oxidative stress.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Alpha-lipoic acid: A promising pharmacotherapy seen through the lens of kidney diseases.Current research in pharmacology and drug discovery · 2024Review
- Short salsalate administration affects cell proliferation, metabolism, and inflammation in polycystic kidney disease.iScience · 2023Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
20 authors at 7 institutions in 3 countries.
Funding
Abstract
Recent studies have reported intrinsic metabolic reprogramming in Pkd1 knock-out cells, implicating dysregulated cellular metabolism in the pathogenesis of polycystic kidney disease. However, the exact nature of the metabolic changes and their underlying cause remains controversial. We show herein that Pkd1
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.